Gastrointestinal Bleeding Part 2


In most patients, the location of the bleed is identified by upper GI endoscopy or colonoscopy. Endoscopy also provides therapeutic options and essential information on the risk of re-bleeding [see Table 3]. There are established visual criteria, based on stigmata of recent hemorrhage, that the endoscopist can use to identify patients at high or low risk for rebleeding.

During upper GI endoscopy, if massive active bleeding is encountered, it is prudent to discontinue the procedure and protect the airway by endotracheal intubation before proceeding. If vi-sualization is impaired, use of large-bore orogastric lavage or a jumbo-channel (6 mm) therapeutic endoscope to evacuate blood and clots may be effective. Erythromycin lactobionate (125 mg intravenously) can also be used to promote quick intestinal transit of blood when active bleeding has stopped.

Table 2 Clinical High-Risk Criteria for Rebleeding and Mortality

Advanced age (a 70 yr)

Major organ comorbidities

In-hospital bleed

Bright-red hematemesis in patient with liver cirrhosis

Hypotension (systolic blood pressure < 100 mm Hg)

Tachycardia (heart rate >100 bpm)

Orthostasis (BP drop > 20 mm Hg; HR rise > 20 bpm)

Hemoglobin < 10 g/dl or drop of a 2 g/dl


Table 3 Endoscopic High-Risk Stigmata for Rebleeding and Indications for Endoscopic Therapy

Nonvariceal bleeding

Arterial spurting

Oozing bleed

Nonbleeding visible vessel

Adherent clot

Variceal bleeding

Large varices (> 5 mm esophageal, > 1 cm gastric)

Red wale marks (longitudinal dilated venules resembling whip marks)

Cherry-red spots (< 2 mm diameter)

Hematocystic spots (> 4 mm diameter)

Before colonoscopy, whenever possible, patients should receive a rapid colonic lavage with 2 to 3 L of a nonabsorbable polyethylene glycol solution administered through a nasogas-tric tube over 2 hours to cleanse the colon and facilitate adequate visualization.


Selective visceral angiography is considered when endoscop-ic therapy for an established lesion has failed and surgery is not an option or when the site of an active bleed remains obscure after endoscopy. An optimal examination with a high positive yield is best obtained when there is active bleeding at rates exceeding 0.5 to 1 ml/min. Significant complications—including contrast reaction, acute renal failure, and femoral artery thrombosis—have been reported in approximately 9% of cases.31,32 The reported sensitivity of angiography varies from 22% to 87%. The specificity approaches 100%.

Radionuclide Technetium Scan

Atechnetium-99m-labeled red cell scan should be considered when active bleeding is suspected but endoscopy has been negative. Nuclear scans can detect bleeding at rates that exceed 0.1 ml/min. On scans, however, pooled blood may sometimes be mistaken for active bleeding, which contributes to a reported false positive rate of about 22%.34 Upper GI bleeding may be mis-diagnosed as lower because of pooling in the distal ileum or right colon. A positive result is more reliable when the scan is done early rather than delayed (several hours later).

Other Measures

Endoscopic techniques that are currently available for examination of the small bowel include push enteroscopy, wireless capsule endoscopy, and intraoperative enteroscopy. Push en-teroscopy typically reaches into the proximal jejunum only, whereas wireless capsule enteroscopy and intraoperative en-teroscopy reach the entire small bowel.

Enteroscopy is currently performed using a pediatric colono-scope with or without an overtube. In one study, the diagnostic yield of enteroscopy in overt GI bleeding was 46%; the most common lesions seen were angiodysplasia and ulcers.35

Wireless capsule endoscopy represents a new technology involving an easily swallowed 11 x 30 mm capsule. No sedation is required. The capsule contains a color video chip, light source, and transmitter. The patient wears an antenna array on a belt. While transiting through the intestine by peristalsis, the capsule takes color photos and sends them to the antenna array. These images are then downloaded onto a computer after the examination. There is a total of 6 to 8 hours of recording time. This technique may be beneficial in patients with recurrent or occult GI bleeding of obscure origin, but it is not appropriate in unstable patients with major active bleeding.

Intraoperative enteroscopy, performed during exploratory lap-arotomy, through single or multiple enterotomy sites, is indicated for the occasional patient with active or recurrent major bleeding of obscure origin. Complications include mucosal laceration, intramural hematoma, mesenteric hemorrhage, and intestinal ischemia.36


Nonvariceal bleeding

Endoscopic Therapy

A variety of endoscopic modalities are currently available for the management of GI bleeding. These can be categorized into thermal, mechanical, and injection devices. Thermal devices are either contact (e.g., heater probe, multipolar electro-cautery) or noncontact (e.g., argon plasma coagulator, laser). These devices generate sufficient heat to create a hemostatic bond through tissue desiccation. The heater probe consists of a Teflon-coated hollow aluminum cylinder with a heating coil. Only heat (no electrical current) is delivered to the tissue. Mul-tipolar or bipolar cautery works by completion of an electrical circuit between two electrodes on the probe tip. The argon plasma coagulator utilizes high-frequency monopolar alternating current delivered to target tissue through ionized argon gas. The conduit of argon gas is called the argon plasma. Electrons flow through a channel of electrically activated, ionized argon gas from the probe electrode to the tissue, causing a thermal effect at the interface. In laser photocoagulation, which is less frequently used, the conversion of light to heat results in coagulation or vaporization of tissue. The neodymium:yttri-um-aluminum-garnet (Nd:YAG) laser is the one most commonly used. Mechanical devices for hemostasis include metallic clips and rubber-band ligators. An injection solution that is generally used to achieve hemostasis is saline mixed with epi-nephrine at a 1:10,000 concentration.

These therapeutic modalities are used alone or in combination. A common practice is to start by injecting epinephrine and saline submucosally in the region of active bleeding so as to stop or slow hemorrhaging and therefore allow for adequate inspection. Thermal or mechanical modalities are then used to achieve definitive hemostasis. Prospective, controlled studies have confirmed the benefit of endoscopic intervention in achieving initial hemostasis and in prevention of rebleeding.37 Combination therapy (i.e., injection plus thermal therapy) has been demonstrated to reduce rebleeding rates more successfully than single therapy.38,39 Currently, combination therapy using injection followed by either a thermal or a mechanical intervention is the most effective approach. Rebleeding after endo-scopic therapy occurs in approximately 20% of cases, typically within 48 to 72 hours after treatment. However, rebleeding can occur as late as 7 days after therapy.


Initial drug therapy for major nonvariceal upper GI bleeding is directed at gastric acid suppression. In a randomized, double-blind study of high-dose omeprazole versus placebo, rebleeding after endoscopic therapy occurred less frequently in the omepra-zole group (7% versus 23%).® In general, proton pump inhibitors are administered in doses that reduce gastric acidity. Blood clot stability depends on intragastric pH, with optimum stability at a pH of 6 or higher.41

In patients with PUD, long-term acid suppression and eradication of H. pylori infection after endoscopic intervention promote ulcer healing, including ulceration at the treatment site, and reduce rebleeding substantially. GI bleeding from NSAIDs is best prevented by avoiding these drugs or by using a cyclooxygenase-2 (COX-2) inhibitor plus a proton pump inhibitor.

Radiologic Intervention

Selective arterial embolization and selective vasoconstriction with intra-arterial infusion of vasopressin are the methods currently available for the control of major nonvariceal GI bleeding. The proponents of embolization favor this form of therapy because it reduces the need for intensive care observation and it eliminates indwelling arterial lines, the risk of catheter dislodge-ment, and problematic systemic side effects of intravenous vaso-pressin [see Pharmacotherapy, below]. Advances in catheter design have allowed for superselective embolization of vasa recta; in experienced units, this modality is probably the treatment of choice. A study of superselective embolization in 48 patients with lower GI bleeding showed that embolization was the definitive treatment in 44% of patients, with a 27% technical failure rate.42 The risks associated with embolization include misplacement of embolic material, inadvertent distal reflux of embolic agent, and excessive devascularization of an organ leading to ischemia and eventual luminal stenosis. Endoscopy can be helpful in determining ischemic injury if suspected. Microcoils (e.g., stainless steel, platinum), gelfoam pledgets, polyvinyl alcohol particles, and collagen suspensions have been used for embolization.

Intra-arterial vasopressin is the drug of choice for selective vasoconstrictive therapy and is generally infused for a minimum of 24 hours. It is associated with a 70% rate of bleeding control and an 18% rate of rebleeding.4345 Vasopressin may be ineffective when bleeding arises from large arteries that do not constrict in response to therapy. A study comparing embolization with va-sopressin showed similar initial hemostasis rates but a higher re-bleeding rate with vasopressin.2 The use of intra-arterial provocative mesenteric angiography with heparin and tissue plasminogen activator (t-PA) to aid in diagnosis has been described but is still in the experimental stage.


Despite the high overall success rate of endoscopic therapy in the treatment of major GI bleeding, surgery is still indicated when (1) initial hemostatic control cannot be achieved, (2) re-bleeding occurs despite repeated endoscopic sessions, (3) a large (> 2 cm) penetrating ulcer is present, (4) a vessel larger than 2 mm in diameter is visible within the culprit lesion, (5) the ulcer is located in the posterior duodenal bulb (this location is associated with the large gastroduodenal artery), and (6) the patient requires substantial transfusion (i.e., four or more units of blood over 24 hours). The choice of surgery depends on the location of the bleed and the presence of comorbidities. Localization of the site of bleeding is critical for surgical planning.

Variceal bleeding Endoscopic Therapy

With variceal bleeding, endoscopic treatment is used primarily for esophageal varices, and the techniques include sclerother-apy and band ligation. Sclerotherapy utilizes a variety of scle-rosants to induce variceal thrombosis, with sodium tetradecyl sulfate and ethanolamine oleate used most frequently. Intra-variceal injections are more effective than paraesophageal injections in controlling bleeding. Compared with a sham injection, sclerotherapy is significantly more likely to stop bleeding (91% versus 60%), reduce mortality during hospitalization (mortality, 25% versus 49%), reduce rebleeding rates (rebleeding, 20% versus 51%), and reduce transfusion need (four versus eight units).46 Complications of sclerotherapy include retrosternal chest pain, fever, ulceration (usually deep ulcers that heal within 3 weeks), dysphagia, delayed perforation (1 to 4 weeks later), and stricture formation. Complication rates vary from 19% to 35% 47-49 The popularity of sclerotherapy has diminished as a result of these complications.

Band ligation is now considered the first-line endoscopic therapy for esophageal varices. The band ligator is readily attached to the distal end of the endoscope, which is advanced to the var-ix; the endoscopist then suctions the varix into the ligator cap and deploys a rubber band around the varix. This results in the plication of the varices and surrounding submucosal tissue, with fibrosis and eventual obliteration of varices. Comparative studies report a better initial control of bleeding (control rates, 91% versus 77%) and lower rebleeding rates (rebleeding, 24% versus 47%) with band ligation than with sclerotherapy.47 Complications of banding include retrosternal chest pain, dysphagia from compromise of the esophageal lumen, band ulceration (usually superficial ulcers that heal within 2 weeks), esophageal injury from the overtube, or esophageal perforation. Complication rates vary from 2% to 19%.50,51

If bleeding continues despite endoscopic therapy or if endo-scopic therapy cannot be initiated, then a modified Sengstaken-Blakemore (Minnesota) tube should be inserted. However, this is only a temporary measure until more definitive treatment—en-doscopic, radiologic, or surgical—can be undertaken.

Preventive measures may be indicated in patients with esophageal varices. Preventive measures are generally offered to patients who have a history of a bleed and to those who have large esophageal varices without a prior bleeding event. Currently, the accepted preventive measures for variceal bleeding include endoscopic band ligation, beta-blocker therapy, or a combination of both. Ligation is performed every 14 to 21 days until varices are completely eradicated, which typically requires three or four sessions.


In acute variceal bleeding, splanchnic blood flow and portal pressure can be reduced by intravenous infusion of vasoconstrictors such as vasopressin, terlipressin, somatostatin, and oc-treotide. Vasopressin is a potent vasoconstrictor that has a reported overall success rate of 50% but a high rebleeding rate when treatment is discontinued.52 It has a short half-life and therefore is given as a continuous infusion. Vasopressin-induced hypertension and bradycardia have the potential to confound hemodynamic monitoring and may give false reassurance in the face of active bleeding. Because the systemic vasoconstrictive side effects associated with vasopressin may lead to myocardial or mesenteric ischemia, it is rarely used alone.

Watermelon stomach with (a) typical spokes of vascular ectasia radiating from the pylorus into the antrum and (b) close-up view.

Figure 7 Watermelon stomach with (a) typical spokes of vascular ectasia radiating from the pylorus into the antrum and (b) close-up view.

To minimize these side effects, it is given in conjunction with nitroglycerin. The ni-troglycerin can be administered as a continuous infusion, sublin-gually, or by transdermal patch. Terlipressin is a synthetic analogue of vasopressin that has fewer side effects and a longer half-life and is given in bolus injections; however, terlipressin has not yet been approved for use in the United States.

Somatostatin, a naturally occurring peptide, is reported to stop variceal bleeding in 80% of patients.17,53 Side effects are few and include hyperglycemia and abdominal pain. Octreotide is a synthetic analogue of somatostatin that is preferred because of its longer half-life. The combination of pharmacologic treatment (e.g., octreotide for 5 days) and endoscopic therapy appear to offer better control of acute bleeding than either alone.

The role of beta blockers is primarily prophylactic. These agents are not used in the acute management of variceal bleeding. The use of isosorbide mononitrate with beta-blocker therapy does not offer a survival advantage and in fact reduces the toler-ability of therapy.

Radiologic Intervention

The radiologic intervention available for variceal bleeding is transjugular intrahepatic portosystemic shunt (TIPS). The accepted indications for TIPS are bleeding or rebleeding that cannot be controlled by either pharmacologic or endoscopic therapy. TIPS is contraindicated in patients with severe hepatic failure, chronic heart failure, hepatic encephalopathy, bile duct obstruction, or cholangitis. TIPS is reported to control bleeding in at least 90% of patients, with rebleeding rates of 12% to 26% at 1 year and 16% to 44% at 2 years.54,55 Patients require close surveillance for shunt dysfunction (evidenced by reduced flow by Doppler ultrasound or reappearance of varices) because primary shunt patency rates are poor (reported cumulative patency rates of 50% at 1 year and 21% at 3 years) but cumulative secondary shunt patency rates can be as satisfactory as 85% and 55% at 1 and 3 years, respectively.55 TIPS should not be undertaken lightly, because the overall procedure-related mortality can be as high as 1% to 2%,54 largely from intraperitoneal hemorrhage. Other complications include hepatic encephalopathy, portal vein thrombosis, renal failure, sepsis, and stent migration or stenosis.

Surgical Intervention

Surgical intervention is rarely used for variceal bleeding; it is considered when other measures have proved ineffective. Surgical treatments include portosystemic venous shunt operations and esophageal devascularization. A variety of surgical shunts are available. These are generally classified as total, partial, or selective, depending on the intended impact of portal flow diversion. The end-to-side portacaval shunt is a total shunt that diverts all portal blood flow into the inferior vena cava. The side-to-side portacaval shunt diverts only a part of the portal blood flow. Selective shunts decompress variceal flow while preserving portal blood flow. The distal splenorenal shunt is a selective shunt designed to prevent encephalopathy, which is often seen with total shunts. Surgical shunts are used for both esophageal and gastric varices. Encephalopathy, accelerated progression of liver failure, and perioperative morbidity can occur with surgical intervention. Esophageal devascularization may be an effective means of controlling acute variceal bleeding, but bleeding can recur as additional varices develop.

Occult Bleeding

The critical metabolic sequela of occult GI bleeding is iron de-ficiency.56 Occult GI bleeding causes most cases of iron deficiency in adults, especially in men and postmenopausal women.


Most of the many lesions that cause overt bleeding can also produce occult blood loss. However, variceal and diverticular hemorrhage invariably bleed overtly, whereas lesions such as watermelon stomach (gastric antral vascular ectasia) and diaphragmat-ic hernia with Cameron erosions tend to bleed occultly. Occult GI bleeding in most patients is suspected only when manifested by fatigue, pallor, or the finding of iron deficiency.

 Evaluation and management of occult gastrointestinal bleeding.

Figure 8 Evaluation and management of occult gastrointestinal bleeding.


In Western countries, erosive or ulcerative diseases of the esophagus, stomach, and duodenum are the most common GI lesions associated with occult bleeding and iron deficiency anemia. Most peptic disease is caused by either H. pylori infection or use of drugs such as aspirin or other NSAIDs. The association between large diaphragmatic hernias and iron deficiency anemia has long been known. A large diaphragmatic hernia is found in about 10% of iron-deficient patients.57 Blood loss in these patients is generally caused by longitudinal mucosal erosions (Cameron erosions) located proximally in the hernia and believed to be secondary to repeated mechanical trauma from respiration.

Cancers and Neoplasms

In adults from Western countries, GI tumors are second only to PUD as a cause of occult bleeding leading to iron deficiency anemia.58 Colorectal cancer is currently the most common source of occult bleeding from GI tract malignancies.

Vascular Causes

Vascular malformations are found in approximately 6% of adults with iron deficiency anemia.59,60 This may be acquired or hereditary (hereditary hemorrhagic telangiectasia). An increasingly recognized and endoscopically treatable vascular lesion is watermelon stomach [see Figure 7], which typically presents as iron deficiency anemia in older women.


When a patient is found to have iron deficiency and occult GI bleeding, it is critical to conduct a thorough GI investigation. Such an evaluation may disclose a health-threatening lesion, in which case specific therapy can be given to prevent associated morbidity and further iron loss. Only after a specific lesion has been treated or has been ruled out, is it appropriate to place patients on iron therapy and monitor them [see Figure 8].

Whatever the culpable lesion, treatment with iron supplementation is important to correct iron deficiency. With conditions such as Cameron erosions, iron supplementation is the mainstay of treatment. Most patients can be managed as outpatients. Oral iron therapy with ferrous sulfate is preferred because it is inexpensive, effective, and, in most cases, well tolerated [see 5:II Red Blood Cell Function and Disorders of Iron Metabolism]. A maximal adult dose of ferrous sulfate is 325 mg three times a day. Absorption is not appreciably increased with higher doses. Oral iron is as effective as parenteral iron in repleting iron stores, except in patients with a malabsorption syndrome, and is safer.

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